Lnc-SNHG16/miR-128 axis modulates malignant phenotype through WNT/β-catenin pathway in cervical cancer cells

Wu, Wu; Guo, Li; Liang, Zhen-Long; Liu, Yuanbin; Yao, Zhi

doi:10.7150/jca.40319

Cited by 38 publications

(37 citation statements)

References 40 publications

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“…In line with our results, Wu et al have showed that miR-128 is downregulated in CC cells, whereas up-regulation of miR-128 obviously suppresses the proliferation, migration, and invasion in CC in vitro. 22 Moreover, we also proved miR-128-3p was a target of MIR4435-2HG. The results implied that miR-128-3p might be regulated by MIR4435-2HG to inhibit the development of CC.…”

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confidence: 69%

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Knockdown of MIR4435-2HG Suppresses the Proliferation, Migration and Invasion of Cervical Cancer Cells via Regulating the miR-128-3p/MSI2 Axis in vitro

Wang

Liu

Jiao

et al. 2020

CMAR

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Long non-coding RNAs (lncRNAs) play major roles in the development of several cancers, including cervical cancer (CC). The purpose of the present study is to explore the regulatory mechanism of MIR4435-2HG on CC in vitro. Patients and Methods: Fifty-nine pairs of CC tissues and adjacent normal tissues were collected from 59 patients by resection. The expression of lncRNA MIR4435-2HG, microRNA (miR)-128-3p and Musashi 2 (MSI2) in CC tissues and cells was detected by quantitative reverse-transcription PCR (qRT-PCR). The viability of CC cells was detected by 3-(4, 5-Dimethyl-2-Thiazolyl)-2, 5-Diphenyl-2-H-Tetrazolium Bromide (MTT) assay. The ability of migration and invasion in CC cells was measured by wound healing assay and transwell invasion assay, respectively. Starbase software and Targetscan software were utilized to predict the relationship between miR-128 and MIR4435-2HG/MSI2, respectively. The dual-luciferase reporter assay was used to confirm these interactions. Results: LncRNA MIR4435-2HG expression was significantly up-regulated in CC tissues (P < 0.001) and cells (P < 0.01). Knockdown of MIR4435-2HG inhibited the proliferation, migration and invasion of CC cells (P < 0.01). MiR-128-3p was a target of MIR4435-2HG and was negatively modulated by MIR4435-2HG (P < 0.0001, r = −0.6331). Up-regulation of miR-128-3p suppressed the proliferation, migration and invasion of CC cells (P < 0.01). In addition, MSI2 was the target gene of miR-128-3p and negatively regulated by miR-128-3p (P < 0.0001, r = −0.4775). Both down-regulation of miR-128-3p and up-regulation of MSI2 reversed the inhibitory effects of MIR4435-2HG knockdown on the proliferation, migration and invasion of CC cells (P < 0.05). Conclusion: MIR4435-2HG knockdown suppresses the proliferation, migration and invasion of CC cells through regulating the miR-128-3p/MSI2 axis, providing a possible therapeutic strategy for CC.

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confidence: 69%

“…21 In addition, miR-128 has been reported to play an anti-cancer role in CC. 22 A recent study has showed that up-regulation of miR-128 conspicuously inhibits the cell viability and epithelial-mesenchymal transition (EMT) procession in CC. 22 However, the regulatory relationship between MIR4435-2HG and miR-128-3p in CC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of MIR4435-2HG Suppresses the Proliferation, Migration and Invasion of Cervical Cancer Cells via Regulating the miR-128-3p/MSI2 Axis in vitro

Wang

Liu

Jiao

et al. 2020

CMAR

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“…miR-128 is closely involved in bone formation-related molecular and signaling pathways, such as Wnt/β-catenin (Fang et al, 2019;Roy et al, 2020;W. Wu et al, 2020), TGF-β (Cai et al, 2017), PI3K/ AKT (Guo et al, 2018;Huo et al, 2019;, AMPK/mTOR (Qi et al, 2020), PPARγ/NF-κB (Qi et al, 2020).…”

Section: Mir-128 and Osteoblastogenesismentioning

confidence: 99%

The emerging role of miR‐128 in musculoskeletal diseases

Shang

Shen

Chen

et al. 2020

Journal Cellular Physiology

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MicroRNA-128 (miR-128) is associated with cell proliferation, differentiation, migration, apoptosis, and survival. Genetic analysis studies have demonstrated that miR-128 participates in bone metabolism, which involves bone marrow-derived mesenchymal stem cells, osteoblasts, osteoclasts, and adipocytes. miR-128 also participates in regeneration of skeletal muscles by targeting myoblast-associated proteins. The deregulation of miR-128 could lead to a series of musculoskeletal diseases. In this review, we discuss recent findings of miR-128 in relation to bone metabolism and muscle regeneration to determine its potential therapeutic effects in musculoskeletal diseases, and to propose directions for future research in this significant field.

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“…[26][27][28] Aberrant miRNA expression is well recognized as a cancer hallmark. It has been reported that some miRNAs involved in the progression and development of cervical cancer, including miR-128, 29 miR-30a, 30 miR-224-3p 31 and miR-186. 32,33 Considering the interaction of lncRNA and miRNA plays an important role in cancer occurrence and progression, 34 it is necessary to clarify the mechanism of lncRNA DLEU2 in cervical cancer by regulating miRNA in cervical cancer.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of LncRNA DLEU2 Inhibits Cervical Cancer Progression via Targeting miR-128-3p

Wang

Hang

et al. 2020

OTT

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Objective: Cervical cancer is one of the most common female malignancies worldwide and represents a major global health challenge. The fast growth of tumor and high rates of metastasis still lead to a poor prognosis of cervical cancer patients. It is urgent to clarify the mechanism and identify predictive biomarkers for the treatment of cervical cancer. Long non-coding RNAs (LncRNAs) have been identified in cervical cancer and are related to malignant phenotypes of cervical cancer cells. However, the roles and mechanism of LncRNA deleted in lymphocytic leukemia (DLEU2) in the tumorigenesis and progression of cervical cancer remain unknown. Materials and Methods: qPCR was performed to analyze the expression of DLEU2, Cyclin D1, CDK4, Bax, Bcl2 and mi-128-3p. Western blot was performed to detect the cell cycle hallmarks expression. CCK8 was used to examine cell proliferation. Cellular apoptosis was analyzed by Hoechst 33,258 staining and AV/PI staining with flow cytometry. Cell cycle was analyzed by flow cytometry. The xenograft model in nude mice was used to elucidate the function of DLEU2 in vivo. Bioinformatics analysis and luciferase reporter assay were proceeded to clarify whether miR-128-3p directly binds with lncRNA DLEU2. Pull-down assay and RNA-binding protein immunoprecipitation assay were used for exploring the relationship between DLEU2 and miR-128-3p. Results: We demonstrated that DLEU2 was upregulated in cervical cancer tumor tissues. Downregulation of DLEU2 inhibited cell proliferation, induced apoptosis and cell cycle arrest at G2/M phase of cervical cancer cells in vitro, and suppressed tumor growth in vivo. Further, LncRNA DLEU2 is one of the targets of miR-128-3p. miR-128-3p inhibitor abrogated the cell proliferation suppressed by knockdown of DLEU2, apoptosis induced by knockdown of DLEU2 and reversed the expression of cell cycle hallmarks regulated by knockdown of DLEU2. Conclusion: Taken together, these results suggested knockdown of DLEU2 inhibited cervical cancer progression via targeting miR-128-3p.

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Lnc-SNHG16/miR-128 axis modulates malignant phenotype through WNT/β-catenin pathway in cervical cancer cells

Cited by 38 publications

References 40 publications

<p>Knockdown of MIR4435-2HG Suppresses the Proliferation, Migration and Invasion of Cervical Cancer Cells via Regulating the miR-128-3p/MSI2 Axis in vitro</p>

<p>Knockdown of MIR4435-2HG Suppresses the Proliferation, Migration and Invasion of Cervical Cancer Cells via Regulating the miR-128-3p/MSI2 Axis in vitro</p>

The emerging role of miR‐128 in musculoskeletal diseases

<p>Knockdown of LncRNA DLEU2 Inhibits Cervical Cancer Progression via Targeting miR-128-3p</p>

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